TY - JOUR
T1 - Modulation of upper airway collapsibility during sleep
T2 - Influence of respiratory phase and flow regimen
AU - Schneider, Hartmut
AU - Boudewyns, An
AU - Smith, Philip L.
AU - O'Donnell, Christopher P.
AU - Canisius, Sebastian
AU - Stammnitz, Axel
AU - Allan, Lawrence
AU - Schwartz, Alan R
PY - 2002/10
Y1 - 2002/10
N2 - We hypothesized that upper airway collapsibility is modulated dynamically throughout the respiratory cycle in sleeping humans by alterations in respiratory phase and/or airflow regimen. To test this hypothesis, critical pressures were derived from upper airway pressure-flow relationships in six tracheostomized patients with obstructive sleep apnea. Pressure-flow relationships were generated by varying the pressure at the trachea and nose during tracheostomy (inspiration and expiration) (comparison A) and nasal (inspiration only) breathing (comparison B), respectively. When a constant airflow regimen was maintained throughout the respiratory cycle (tracheostomy breathing), a small yet significant decrease in critical pressure was found at the inspiratory vs. end- and peak-expiratory time point [7.1 ± 1.6 (SE) to 6.6 ± 1.9 to 6.1 ± 1.9 cmH2O, respectively; P < 0.05], indicating that phasic factors exerted only a modest influence on upper airway collapsibility. In contrast, we found that the inspiratory critical pressure fell markedly during nasal vs. tracheostomy breathing [1.1 ± 1.5 (SE) vs. 6.1 ± 1.9 cmH2O; P < 0.01], indicating that upper airway collapsibility is markedly influenced by differences in airflow regimen. Tracheostomy breathing was also associated with a reduction in both phasic and tonic genioglossal muscle activity during sleep. Our findings indicate that both phasic factors and airflow regimen modulate upper airway collapsibility dynamically and suggest that neuromuscular responses to alterations in airflow regimen can markedly lower upper airway collapsibihty during inspiration.
AB - We hypothesized that upper airway collapsibility is modulated dynamically throughout the respiratory cycle in sleeping humans by alterations in respiratory phase and/or airflow regimen. To test this hypothesis, critical pressures were derived from upper airway pressure-flow relationships in six tracheostomized patients with obstructive sleep apnea. Pressure-flow relationships were generated by varying the pressure at the trachea and nose during tracheostomy (inspiration and expiration) (comparison A) and nasal (inspiration only) breathing (comparison B), respectively. When a constant airflow regimen was maintained throughout the respiratory cycle (tracheostomy breathing), a small yet significant decrease in critical pressure was found at the inspiratory vs. end- and peak-expiratory time point [7.1 ± 1.6 (SE) to 6.6 ± 1.9 to 6.1 ± 1.9 cmH2O, respectively; P < 0.05], indicating that phasic factors exerted only a modest influence on upper airway collapsibility. In contrast, we found that the inspiratory critical pressure fell markedly during nasal vs. tracheostomy breathing [1.1 ± 1.5 (SE) vs. 6.1 ± 1.9 cmH2O; P < 0.01], indicating that upper airway collapsibility is markedly influenced by differences in airflow regimen. Tracheostomy breathing was also associated with a reduction in both phasic and tonic genioglossal muscle activity during sleep. Our findings indicate that both phasic factors and airflow regimen modulate upper airway collapsibility dynamically and suggest that neuromuscular responses to alterations in airflow regimen can markedly lower upper airway collapsibihty during inspiration.
KW - Collapsibility
KW - Critical pressure
KW - Obstructive sleep apnea
KW - Tracheostomy
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U2 - 10.1152/japplphysiol.00942.2001
DO - 10.1152/japplphysiol.00942.2001
M3 - Article
C2 - 12235037
AN - SCOPUS:0036785909
VL - 93
SP - 1365
EP - 1376
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
SN - 0161-7567
IS - 4
ER -